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Biochemistry 2 > ETC and Oxidative Phosphorylation > Flashcards

ETC and Oxidative Phosphorylation Flashcards

1
Q

what organelle produces ATP?

A

mitochondria

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2
Q

mitochondria anatomy

A

inner and outer membrane

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3
Q

where does oxidative phosphorylation occur?

A

inner mitochondrial membrane

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4
Q

what is oxidative phosphorylation (meaning of each word)?

A 
oxidation = molecules give up electrons
phosphorylation = addition of phosphate group to ADP to make ATP
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5
Q

oxidative phosphorylation overview sentence

A

make ATP by donating electrons to complexes in the inner mitochondrial membrane

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6
Q

what are the complexes?

A

proteins or lipids coupled with metals (EX: iron and copper)

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7
Q

what is the final electron acceptor

A

oxygen

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8
Q

overall purpose of oxidative phosphorylation?

A

create a proton gradient which is used to create ATP

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9
Q

What does ETC start with?

A

NADH and FADH2

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10
Q

where do we get NADH and FADH2 from?

A

1) glycolysis in cytoplasm
2) citric acid cycle in mitochondria
3) fatty acid oxidation in mitochondria

dehydrogenases help generate NADH and FADH2

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11
Q

how do NADH and FADH2 from cytoplasm (glycolysis) enter mitochondria for ETC?

A

the malate-aspartate shuttle (enter as NADH)

glycerol-3-phosphate shuttle (enter ETC at FADH2)

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12
Q

1st point of entry into ETC

A

Complex 1
contains flavin mononucleotide
and iron-sulfur centers (FeS)
NADH gives electron to NAD+

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13
Q

what can we do with NAD+ created by complex I

A

can be re-used by dehydrogenases to create more NADH

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14
Q

2nd point of entry into ETC

A

FADH2 donates electron to complex II and becomes FAD+

complex II = succinate dehydrogenase

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15
Q

relationship between CAC and ETC

A

they share a step! complex II (succinate dehydrogenase is also in CAC)
their activity rises and falls together

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16
Q

where do electrons from complex I and II go?

A

coenzyme Q (ubiquinone)

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17
Q

what is coenzyme Q

A

cholesterol derivative

it is the only lipid in the ETC

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18
Q

where does coenzyme Q send the electrons?

A

cytochromes! (Complex III)

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19
Q

what are cytochromes?

A

proteins with heme groups (contain iron)

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20
Q

heme group rxn

A

1) iron accepts an electron and goes from Fe3+ to Fe2+

2) iron releases electron to next cytochrome in chain and becomes Fe3+ again

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21
Q

complex III is made up of

A

cytochrome b and cytochrome c1

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22
Q

after complex III, electrons go to?

A

cytochrome c, then complex IV

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23
Q

complex IV is made up of?

A

cytochrome a and cytochrome a3 (together are called cytochrome oxidase)

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24
Q

what does cytochrome oxidase do?

A

transfer electrons to final electron acceptor (oxygen)

oxygen becomes electronegative enough to grab 2 protons and make water

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25
Q

what happens in hypoxia (no oxygen)

A

ETC is interrupted, ATP synthesis doesn’t happen

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26
Q

what does ETC produce?

A

the passing of electrons creates an electrical current which provides energy that allows protons to be pumped out of the mitochondria and into the space between the outer and inner mito membrane

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27
Q

which complexes span the inner mitochondrial membrane?

A

1, 3, and 4

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28
Q

how do complexes push protons?

A

as electrons move through, the complexes change conformation to push protons across

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29
Q

what do protons use to get across the mito membrane?

A

mito membrane is impermeable to protons

they use F0 proton channel attached to enzyme F1

30
Q

what is F1

A

an ATP synthase that uses proton gradient to phosphorylate ADP into ATP
sometimes called complex V

31
Q

ADP/ATP antiport

A

pumps protons out of mitochondria and into cytoplasm

ATP leaves, a new ADP goes in to start cycle again

32
Q

energy payoff for NADH

A

1 NADH makes 3 ATP

this is bc NADH activates 3 proton pumps (1, 3, and 4)

33
Q

energy payoff for FADH2

A

1 FADH2 makes 2 ATP

bc it skips complex 1

34
Q

those payoffs are called

A

P/O (phosphate: oxygen) ratios

bc they require oxygen as final electron acceptor

35
Q

P/O ratio

A

rate of ATP produced per oxygen consumed for each molecule

these are approximates

36
Q

is ETC under hormonal control?

A

NO!

it is controlled by energy levels

37
Q

high ATP

A

slow down ETC

38
Q

high ADP

A

means low energy, speeds up ETC

39
Q

drugs do what to OX phos

A

break it up via uncoupling or inhibition

40
Q

uncoupling

A

ETC is normally coupled with ATP synthesis (they happen together)
uncoupling agents break this link by inserting their own proton channels (ionophores) inter inner mitochondrial membrane or by carrying protons back into mito matrix

41
Q

uncoupling agents cause bypass of what?

A

F0 (now F1 can’t phosphorylate ADP into ATP)

they dissipate proton gradient

42
Q

uncoupling agents where do electrons flow

A

electrons still flow up to oxygen
red blood cells still deliver oxygen to tissues
As ADP levels rise, body tries to make more NADH and FADH2
this is useless!

43
Q

extra energy

A

we don’t use electron’s energy to move it across inner mito membrane, so more of that energy becomes heat energy

44
Q

endogenous uncoupling agents

A

thermogenin

45
Q

thermogenin

A

in brown adipose tissue of babies
used to generate heat
also found in hibernating animals
aka uncoupling protein 1 (UCP1)

46
Q

drug that is an uncoupling agent

A 
high doses of aspirin
leads to high metabolic rate
causes metabolic acidosis
if ATP gets too low, this leads to respiratory acidosis
(combination is life threatening)
47
Q

inhibition

A

chemicals/drugs inhibit components of ETC
STOPS flow of electrons through ETC
leads to decrease in ATP synthesis

48
Q

what builds up during inhibition?

A

electron donors: NADH and FADH2
this means body will stop making more
metabolic rate falls

49
Q

poisons that inhibit ETC

A

lead to death quickly
carbon monoxide, cyanide (inhibit complex IV)
barbiturates (GABA agonists for seizure disorders) (inhibit complex I in high doses)
oligomycin inhibits F0 component of ATP synthase

50
Q

statins

A

decrease synthesis of coenzyme Q
decreases ATP synthesis
can lead to muscle pains and crams

51
Q

mitochondria inner membrane…why is it folded?

A

to increase surface area for ETC!

52
Q

as electrons go through chain, they

A

fall in energy and move toward progressively more positive reduction potentials

53
Q

electron movement in Complex I

A

1) NADH binds Complex I
2) electrons move to FMN to Fe-S clusters
3) electrons reduce UQ to UQH2

54
Q

MPP+

A

MPP+ inhibits complex I
monoamine oxidase B (enzyme that creates MPP+) acts preferentially in cells of brain that produce dopamine (Parkinson’s!)

55
Q

Redox carriers in complex II

A

1) FAD picks up electrons from succinate

2) electrons move through carriers until picked up by UQ

56
Q

complex III overview

A

picks up electrons from UQH2 and gives them to cytochrome c (uses Q cycle)

57
Q

electron carriers in complex III

A

cytochrome bL
cytochrome bH
cytochrome c1
Fe-S protein

58
Q

cytochrome c

A

peripheral membrane protein that brings electrons to complex IV
heme c is linked to it

59
Q

Q cycle

A

in complex III

allows translocation of H+ across membrane as electrons are transferred between carriers

60
Q

Q cycle net rxn

A

every 2 UQH2, 4 H+ cross membrane and 2 H+ regenerate UQH2

61
Q

complex IV electron movement

A

in reduction of O2 to 2H2O (4 electrons):
4H+ used to reduce oxygen to water
4 H+ moved across membrane
8 H+ leave the matrix

62
Q

chemiosmotic hypothesis

A

energy from electron transfer is stored in formation of proton gradient
energy in proton gradient is coupled to ATP synthesis

63
Q

F0 subunit

A

protons move through rotor (F0) which turns F1 subunit (the sphere)

64
Q

C ring

A

Each subunit binds a proton to turn C ring

Fewer C subunits you have, fewer protons it takes for a 360 degree rotation

65
Q

energy requiring step of ATP synthesis

A

ATP release from ATP synthase requires most energy

ATP synthesis itself doesn’t require energy

66
Q

flow of protons through ATP synthase

A

flow of protons through F0 subunit causes rotation of F- plus gamma.
This rotation drives conformational changes in beta subunits that mediate binding of substrates, ATP synthesis, and release of ATP.

67
Q

proton gradient requirements (2)

A

functional ETC and a proton-impermeable membrane

68
Q

ETC and ATP synthesis inhibits

A

if one is inhibited, so is the other

EX: cyanide, azide, carbon monoxide, demerol, amytal

69
Q

ATP-ADP translocase

A

moves ADP into mito matrix and ATP out of mito matrix

70
Q

malate-aspartate shuttle

A

Malate to mitochondrial matrix
Malate to oxaloacetate
Oxaloacetate then leaves mitochondria as aspartate to reset the cycle
In cytoplasm aspartate then becomes oxaloacetate again

71
Q

glycerophosphate shuttle

A

transfers NADH in cytosol to mitochondria since inner mito membrane is impermeable to NADH and NAD+

72
Q

Pasteur effect

A

Yeast metabolizing glucose, they use a lot more glucose under anaerobic than aerobic conditions (bc they still need to regenerate NAD+)
BUT with no oxygen it’s hard to regenerate NAD+
Anaerobic glycolysis = 2 ATP
Aerobic glycolysis = 32-34 ATP
Aerobic allows them to consume less glucose to get more energy

Biochemistry 2 (32 decks)

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